Our research is directed toward understanding the processes that control mitochondrial motility and determining the contribution of mitochondria to the Parkinson's disease process.

In order to study mitochondrial movement ("mitochondrial trafficking") we use fluorescence microscopy to monitor the behaviour of mitochondria in live neuron cultures.  Using recombinant DNA technology, we can introduce fluorescent proteins into neuronal cultures which specifically label mitochondria.  This causes the mitochondria to "glow" when a certain wavelength of light is shone on them, and allows us to monitor the behaviour of individual mitochondria in living cells. To capture the behaviour of mitochondria, we employ a digital fluorescence microscopy system; a special microscope specifically designed to view fluorescent events inside living cells.  Using this system we can examine if compromise of mitochondrial trafficking is a contributing factor to the development of Parkinson's disease.

Our study of the involvement of mitochondria in Parkinson's disease also examines the contribution of "oxidative stress". Oxidative stress is a term used to describe the excessive production of highly chemically-reactive oxygen-containing compounds. Oxidative stress has been associated with the aging process in neurons, and is thought to be a contributing factor to the selective loss of neurons observed in Parkinson's disease and other neurodegenerative disorders. We have developed a cell culture model in which we can examine changes in the motility of mitochondria in response to chronic (prolonged) oxidative stress. Cultures of neurons are exposed to oxidative stress over a long period of time to simulate the chronic oxidative stress associated with aging.

Utilizing our cell culture model we propose to characterize the dynamic responses of mitochondria to chronic oxidative stress and subsequent cell death in Parkinson's disease models. We hypothesize that chronic oxidative stress impairs energy delivery by mitochondria and thereby makes neurons more susceptible to degeneration. In addition, using molecular biology tools, we can directly impair the motility of mitochondria in neuronal cultures. We can then examine whether inhibiting mitochondrial motility increase the susceptibility of neurons to degeneration using cell culture models of Parkinson's disease.

The goal of our research is to provide new insights into the underlying causes of neurodegenerative disorders like Parkinson's disease. By determining the cellular mechanisms of the disease, we hope to provide targets for therapeutic treatment of the disease. These studies will also yield insights into why older brains are more susceptible to neurodegenerative disorders such as Parkinson's disease, and perhaps lead to preventative therapies.